P4796 - Unorthodox Alcoholic Liver Injury

Simardeep Singh, MBBS¹, Avneet Kaur, MBBS¹, Greeshma N Gaddipati, MBBS¹, Joseph Atarere, MD, MPH¹, Boniface Mensah, MBChB, MPH¹, Ramya Vasireddy, MBBS¹, Kavneet Gill, MD^2
1MedStar Union Memorial Hospital, Baltimore, MD; ²MedStar Franklin Square Medical Center, Baltimore, MD

Introduction: Alcoholic liver disease (ALD) can progress from fatty liver to steatohepatitis, fibrosis, cirrhosis, and rarely hepatocellular carcinoma. Typically, ALD leads to elevation in aminotransferases (AST and ALT) but biliary duct involvement in atypical cases can cause significant elevations in ductal enzymes. We present a rare case of ALD in a 58-year-old man with chronic alcohol use developing alcoholic hepatitis with cholestasis. Recognizing ALD deviations from typical liver enzyme patterns is crucial for prompt diagnosis and treatment.

Case Description/Methods: A 58-year-old man with opiate dependence presented with jaundice, pruritus, and fatigue, reporting heavy alcohol use of over 180 gm of whiskey daily for 20 years. Initial assessment showed sinus tachycardia, hypertension, elevated AST/ ALT 472/301, hyperbilirubinemia (15.9), direct bilirubin (13), ALP (904), and ethanol levels (94). USG revealed hepatomegaly. With a MELD score of 21, he had a 19% three-month mortality risk. Cholestyramine and hydroxyzine were started. Transaminitis improved, but ALP remained elevated, and total bilirubin increased to 18. MRI was not done due to claustrophobia. Hepatitis panel was negative for HAV and HBV, and positive for HCV antibodies with a negative viral load, indicating resolved infection. Autoimmune markers (SMA and AMA) were negative. Iron studies and AFP were normal. High ceruloplasmin (47) and ferritin (459.7 ng/ml) suggested an acute phase reaction. Despite management, bilirubin persisted at 19.9. A triple-phase CT ruled out hepatic lesions. Liver biopsy showed alcohol-related steatohepatitis and stage 2 fibrosis.

Discussion: ALD remains a significant US health concern with high mortality and transplant needs. Alcoholic hepatitis is diagnosed by jaundice within 60 days of heavy alcohol use, elevated bilirubin and AST levels, and an AST/ALT ratio >2, with no other identifiable causes. Alcohol-induced cholestasis mechanisms include bile transport interference, direct duct epithelial cells, and hepatocyte damage. Maddrey's discriminant function (MDF) guides severe AH assessment (MDF ≥32), often requiring corticosteroid therapy due to high short-term morbidity and mortality. Corticosteroids mitigate inflammation and oxidative stress from chronic alcoholism. Adjunctive therapies like antioxidant cocktails are under investigation but lack conclusive evidence. Early recognition and alcohol abstinence are crucial, highlighting the further need for research into novel therapeutics—Grammar checked by AI.


Disclosures:


Simardeep Singh, MBBS¹, Avneet Kaur, MBBS¹, Greeshma N Gaddipati, MBBS¹, Joseph Atarere, MD, MPH¹, Boniface Mensah, MBChB, MPH¹, Ramya Vasireddy, MBBS¹, Kavneet Gill, MD². P4796 - Unorthodox Alcoholic Liver Injury, ACG 2024 Annual Scientific Meeting Abstracts. Philadelphia, PA: American College of Gastroenterology.